Depolarization-induced suppression of excitation in murine autaptic hippocampal neurones
Depolarization-induced suppression of excitation and inhibition (DSE and DSI) appear to be important forms of short-term retrograde neuronal plasticity involving endocannabinoids (eCB) and the activation of presynaptic cannabinoid CB1 receptors. We report here that CB1-dependent DSE can be elicited...
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| Veröffentlicht in: | The Journal of physiology 2005-12, Vol.569 (2), p.501-517 |
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| description | Depolarization-induced suppression of excitation and inhibition (DSE and DSI) appear to be important forms of short-term retrograde
neuronal plasticity involving endocannabinoids (eCB) and the activation of presynaptic cannabinoid CB1 receptors. We report
here that CB1-dependent DSE can be elicited from autaptic cultures of excitatory mouse hippocampal neurones. DSE in autaptic
cultures is both more robust and elicited with a more physiologically relevant stimulus than has been thus far reported for
conventional hippocampal cultures. An additional requirement for autaptic DSE is filled internal calcium stores. Pharmacological
experiments favour a role for 2-arachidonyl glycerol (2-AG) rather than arachidonyl ethanolamide (AEA) or noladin ether as
the relevant endocannabinoid to elicit DSE. In particular, the latter two compounds fail to reversibly inhibit EPSCs, a quality
inconsistent with the role of bona fide eCB mediating DSE. Î 9 -Tetrahydrocannabinol (Î 9 -THC) fails to inhibit EPSCs, yet readily occludes both DSE and EPSC inhibition by a synthetic CB1 agonist, WIN 55212-2. With
long-term exposure (â¼18 h), Î 9 -THC also desensitizes CB1 receptors. Lastly, a functional endocannabinoid transporter is necessary for the expression of
DSE. |
| doi_str_mv | 10.1113/jphysiol.2005.091918 |
| format | Article |
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neuronal plasticity involving endocannabinoids (eCB) and the activation of presynaptic cannabinoid CB1 receptors. We report
here that CB1-dependent DSE can be elicited from autaptic cultures of excitatory mouse hippocampal neurones. DSE in autaptic
cultures is both more robust and elicited with a more physiologically relevant stimulus than has been thus far reported for
conventional hippocampal cultures. An additional requirement for autaptic DSE is filled internal calcium stores. Pharmacological
experiments favour a role for 2-arachidonyl glycerol (2-AG) rather than arachidonyl ethanolamide (AEA) or noladin ether as
the relevant endocannabinoid to elicit DSE. In particular, the latter two compounds fail to reversibly inhibit EPSCs, a quality
inconsistent with the role of bona fide eCB mediating DSE. Î 9 -Tetrahydrocannabinol (Î 9 -THC) fails to inhibit EPSCs, yet readily occludes both DSE and EPSC inhibition by a synthetic CB1 agonist, WIN 55212-2. With
long-term exposure (â¼18 h), Î 9 -THC also desensitizes CB1 receptors. Lastly, a functional endocannabinoid transporter is necessary for the expression of
DSE.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2005.091918</identifier><identifier>PMID: 16179366</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Animals ; Arachidonic Acids - pharmacology ; Benzoxazines ; Calcium - physiology ; Cannabinoid Receptor Modulators - metabolism ; Cannabinoid Receptor Modulators - physiology ; Cell Physiology ; Cells, Cultured ; Dronabinol - pharmacology ; Endocannabinoids ; Excitatory Postsynaptic Potentials - drug effects ; Excitatory Postsynaptic Potentials - physiology ; Glutamic Acid - physiology ; Glycerides - pharmacology ; Hippocampus - cytology ; Hippocampus - physiology ; Mice ; Mice, Inbred C57BL ; Morpholines - pharmacology ; Naphthalenes - pharmacology ; Neuronal Plasticity - drug effects ; Neuronal Plasticity - physiology ; Neurons - metabolism ; Neurons - physiology ; Nitric Oxide - physiology ; Patch-Clamp Techniques ; Polyunsaturated Alkamides ; Receptor, Cannabinoid, CB1 - antagonists & inhibitors ; Receptor, Cannabinoid, CB1 - physiology</subject><ispartof>The Journal of physiology, 2005-12, Vol.569 (2), p.501-517</ispartof><rights>2005 The Journal of Physiology © 2005 The Physiological Society</rights><rights>The Physiological society 2005 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5858-ffbe90e5b1c78f30bb47f4e3f3d647c5ba0e651761271e46aacbdd94d62792f83</citedby><cites>FETCH-LOGICAL-c5858-ffbe90e5b1c78f30bb47f4e3f3d647c5ba0e651761271e46aacbdd94d62792f83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464237/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464237/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16179366$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Straiker, Alex</creatorcontrib><creatorcontrib>Mackie, Ken</creatorcontrib><title>Depolarization-induced suppression of excitation in murine autaptic hippocampal neurones</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Depolarization-induced suppression of excitation and inhibition (DSE and DSI) appear to be important forms of short-term retrograde
neuronal plasticity involving endocannabinoids (eCB) and the activation of presynaptic cannabinoid CB1 receptors. We report
here that CB1-dependent DSE can be elicited from autaptic cultures of excitatory mouse hippocampal neurones. DSE in autaptic
cultures is both more robust and elicited with a more physiologically relevant stimulus than has been thus far reported for
conventional hippocampal cultures. An additional requirement for autaptic DSE is filled internal calcium stores. Pharmacological
experiments favour a role for 2-arachidonyl glycerol (2-AG) rather than arachidonyl ethanolamide (AEA) or noladin ether as
the relevant endocannabinoid to elicit DSE. In particular, the latter two compounds fail to reversibly inhibit EPSCs, a quality
inconsistent with the role of bona fide eCB mediating DSE. Î 9 -Tetrahydrocannabinol (Î 9 -THC) fails to inhibit EPSCs, yet readily occludes both DSE and EPSC inhibition by a synthetic CB1 agonist, WIN 55212-2. With
long-term exposure (â¼18 h), Î 9 -THC also desensitizes CB1 receptors. Lastly, a functional endocannabinoid transporter is necessary for the expression of
DSE.</description><subject>Animals</subject><subject>Arachidonic Acids - pharmacology</subject><subject>Benzoxazines</subject><subject>Calcium - physiology</subject><subject>Cannabinoid Receptor Modulators - metabolism</subject><subject>Cannabinoid Receptor Modulators - physiology</subject><subject>Cell Physiology</subject><subject>Cells, Cultured</subject><subject>Dronabinol - pharmacology</subject><subject>Endocannabinoids</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Glutamic Acid - physiology</subject><subject>Glycerides - pharmacology</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Morpholines - pharmacology</subject><subject>Naphthalenes - pharmacology</subject><subject>Neuronal Plasticity - drug effects</subject><subject>Neuronal Plasticity - physiology</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>Nitric Oxide - physiology</subject><subject>Patch-Clamp Techniques</subject><subject>Polyunsaturated Alkamides</subject><subject>Receptor, Cannabinoid, CB1 - antagonists & inhibitors</subject><subject>Receptor, Cannabinoid, CB1 - physiology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkkuP1SAYhonROMfRf2BMV7rqESiXsjEx43jLJLoYE3eE0q9TJi0gtI5nfr2tPd5WumLB8z7A94LQY4L3hJDq-XXsD9mFYU8x5nusiCL1HbQjTKhSSlXdRTuMKS0ryckJepDzNcakwkrdRydEkIUQYoc-v4IYBpPcrZlc8KXz7WyhLfIcY4K8HOCL0BXwzbrpB1E4X4xzch4KM08mTs4WvYsxWDNGMxQe5hQ85IfoXmeGDI-O6yn69Pr88uxtefHhzbuzlxel5TWvy65rQGHgDbGy7ircNEx2DKquagWTljcGg-BECkIlASaMsU3bKtYKKhXt6uoUvdi8cW5GaC34KZlBx-RGkw46GKf_3vGu11fhq14GxWglF8HToyCFLzPkSY8uWxgG4yHMWYu65myd-L9AIhmRvF5BtoE2hZwTdL9uQ7BeTfpnd3rtTm_dLbEnf77kd-hY1gKoDbhxAxz-S6ov338klK7yZ1u2d1f9jUugNzoH62A6aC6UppovP-Q7jk27kw</recordid><startdate>200512</startdate><enddate>200512</enddate><creator>Straiker, Alex</creator><creator>Mackie, Ken</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200512</creationdate><title>Depolarization-induced suppression of excitation in murine autaptic hippocampal neurones</title><author>Straiker, Alex ; Mackie, Ken</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5858-ffbe90e5b1c78f30bb47f4e3f3d647c5ba0e651761271e46aacbdd94d62792f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Arachidonic Acids - pharmacology</topic><topic>Benzoxazines</topic><topic>Calcium - physiology</topic><topic>Cannabinoid Receptor Modulators - metabolism</topic><topic>Cannabinoid Receptor Modulators - physiology</topic><topic>Cell Physiology</topic><topic>Cells, Cultured</topic><topic>Dronabinol - pharmacology</topic><topic>Endocannabinoids</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Glutamic Acid - physiology</topic><topic>Glycerides - pharmacology</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Morpholines - pharmacology</topic><topic>Naphthalenes - pharmacology</topic><topic>Neuronal Plasticity - drug effects</topic><topic>Neuronal Plasticity - physiology</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Nitric Oxide - physiology</topic><topic>Patch-Clamp Techniques</topic><topic>Polyunsaturated Alkamides</topic><topic>Receptor, Cannabinoid, CB1 - antagonists & inhibitors</topic><topic>Receptor, Cannabinoid, CB1 - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Straiker, Alex</creatorcontrib><creatorcontrib>Mackie, Ken</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Straiker, Alex</au><au>Mackie, Ken</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Depolarization-induced suppression of excitation in murine autaptic hippocampal neurones</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2005-12</date><risdate>2005</risdate><volume>569</volume><issue>2</issue><spage>501</spage><epage>517</epage><pages>501-517</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Depolarization-induced suppression of excitation and inhibition (DSE and DSI) appear to be important forms of short-term retrograde
neuronal plasticity involving endocannabinoids (eCB) and the activation of presynaptic cannabinoid CB1 receptors. We report
here that CB1-dependent DSE can be elicited from autaptic cultures of excitatory mouse hippocampal neurones. DSE in autaptic
cultures is both more robust and elicited with a more physiologically relevant stimulus than has been thus far reported for
conventional hippocampal cultures. An additional requirement for autaptic DSE is filled internal calcium stores. Pharmacological
experiments favour a role for 2-arachidonyl glycerol (2-AG) rather than arachidonyl ethanolamide (AEA) or noladin ether as
the relevant endocannabinoid to elicit DSE. In particular, the latter two compounds fail to reversibly inhibit EPSCs, a quality
inconsistent with the role of bona fide eCB mediating DSE. Î 9 -Tetrahydrocannabinol (Î 9 -THC) fails to inhibit EPSCs, yet readily occludes both DSE and EPSC inhibition by a synthetic CB1 agonist, WIN 55212-2. With
long-term exposure (â¼18 h), Î 9 -THC also desensitizes CB1 receptors. Lastly, a functional endocannabinoid transporter is necessary for the expression of
DSE.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>16179366</pmid><doi>10.1113/jphysiol.2005.091918</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Free Content; MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Arachidonic Acids - pharmacology Benzoxazines Calcium - physiology Cannabinoid Receptor Modulators - metabolism Cannabinoid Receptor Modulators - physiology Cell Physiology Cells, Cultured Dronabinol - pharmacology Endocannabinoids Excitatory Postsynaptic Potentials - drug effects Excitatory Postsynaptic Potentials - physiology Glutamic Acid - physiology Glycerides - pharmacology Hippocampus - cytology Hippocampus - physiology Mice Mice, Inbred C57BL Morpholines - pharmacology Naphthalenes - pharmacology Neuronal Plasticity - drug effects Neuronal Plasticity - physiology Neurons - metabolism Neurons - physiology Nitric Oxide - physiology Patch-Clamp Techniques Polyunsaturated Alkamides Receptor, Cannabinoid, CB1 - antagonists & inhibitors Receptor, Cannabinoid, CB1 - physiology |
| title | Depolarization-induced suppression of excitation in murine autaptic hippocampal neurones |
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